Nitric oxide formation versus scavenging: the red blood cell balancing act
Open accessAbstract
Nitric oxide (NO) is a key modulator of vascular homeostasis controlling critical functions related to blood flow, respiration, cell death and proliferation, and protecting the vasculature from pro-inflammatory and coagulative stresses. Inhibition of NO formation, and/or diversion of NO away from its physiological signalling targets lead to dysregulated NO bioavailability, a hallmark of numerous vascular and pulmonary diseases. Current concepts suggest that the balance between NO formation and NO scavenging is critical in disease development, with the corollary being that redressing the balance offers a target for therapeutic intervention. Evidence presented over the last two decades has seen red blood cells (RBCs) and haemoglobin specifically emerge as prominent effectors in this paradigm. In this symposium review article, we discuss recent insights into the mechanisms by which RBCs may modulate the balance between NO-formation and inhibition. We discuss how these mechanisms may become dysfunctional to cause disease, highlight key questions that remain, and discuss the potential impact of these insights on therapeutic opportunities.
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The relative contribution of either mechanism to NO formation is likely to vary with oxygen partial pressure along the vascular tree.
“The relative contribution of either mechanism to NO formation is likely to vary with oxygen partial pressure along the vascular tree [86,87].”
From On the chemical biology of the nitrite/sulfide interaction (2015) · cites this paper as [87]
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References 66 · Cited by 48
- Authors
- Owusu, B. Y., Stapley, R., & Patel, R. P.
- Affiliations
- University of Alabama at Birmingham (US)
- Corresponding author
- Patel, Rakesh P.
- ORCID
- Patel, Rakesh P.
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2012-07-27
- Volume
- 590
- Issue
- 20
- Pages
- 4993-5000
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC3497558
- OpenAlex
- W2126050049
- Cited by
- 48
- References
- 66
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 1 · 2022: 1 · 2021: 7 · 2020: 5 · 2019: 2 · 2018: 1 · 2017: 3 · 2016: 4 · 2015: 4 · 2014: 6 · 2013: 7 · 2012: 3
- FWCI
- 0.70
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL095468, HL092624, R01HL092624, HL095468)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hemoglobin structure and function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heme Oxygenase-1 and Carbon Monoxide
- Keywords
- nitric oxide, nitric oxide production, nitric oxide scavenging, erythrocytes, hemoglobin, NO bioavailability, vascular homeostasis, vascular disease, lung disease, therapeutic target
- MeSH terms
- Animals, Erythrocytes, Hemoglobins, Humans, Nitric Oxide, Nitrites
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